Vascular diseases that cause clogging of arteries are the primary killer of adults in the United States. The clogging of arteries is due to an accumulation of lipids, cholesterol clots, etc., within the artery walls. The accumulation of clogging material may be accelerated by hypertension, high cholesterol, smoking and other well know risk factors. Medical researchers have therefore focused extensively on the cardiovascular system's physiology, functioning and disorders to prevent an the devastating ubiquitous disease referred to as atherosclerosis.
The study of atherosclerosis involves the study of the left ventricle and its contingent arterial system. The left ventricle is a muscular pumping chamber that pumps blood into the arterial system under high pressure. As the ventricle contracts and ejects blood into the arterial system the pressure level is dictated by the rate at which the ventricle contracts, the compliance of the vascular system, the ventricular volume, the viscosity of the blood, and the resistance of the distal capillary bed. Young persons have highly compliant vascular systems. This provides a capacitive effect that reduces peak pressure and smoothes the pulsatility of the blood flow. In adults the arteries become less compliant, thereby reducing the capacitive smoothing effect. In short, with age the blood flows at higher pressure and is more highly pulsatile.
The loss of compliance causes several related effects, namely, the peak pressure rises and the rate of change of velocity with time increases. These effects are believed to cause injury to the tissue in the artery wall, and may be the etiology of the clogging of arteries, i.e., arteriosclerosis and atherosclerosis. In particular, it is believed that the highly pulsatile flow in non-compliant vascular systems (which we call "bolus pumping" stresses the vascular system in various ways. For example, such action results in pressure induced stress and shear induced stress, with the amount of induced stress being a function of several factors, e.g., rate of change of the velocity of the blood, blood pressure, blood viscosity, red blood cell deformability. The stresses induced under bolus pumping cause the body's injury response mechanisms to react to heal the injury to maintain structural integrity, but this reaction interferes with the functionality of the artery. In short, because the artery protects itself from future injury, the artery becomes less functional.
For example, if the left ventricle ejection over stretches the aorta (e.g., as a result of elevated peak systolic pressure) injury will occur to the arterial wall. The aorta will respond in turn by thickening, hardening and becoming less compliant--medically termed "arteriosclerosis." Logically this process should first effect the region of the vascular system that is overstretched first, i.e., the aortic arch and adjacent branches due to their proximity to the left ventricle, and the peripheral vascular system (where the effects of gravity accentuates the pressure causing overstretching). These areas are where arteriosclerosis typically develops first, causing heart attacks, strokes, and necessitating the amputation of legs.
Shear stress is believed to be the underlying cause of clogging of the arteries--medically termed "atherosclerosis." In this regard bolus pumping with its highly pulsatile flow (which we call "bolus flow") is believed to induce injury to the intima. In particular, we believe that bolus flow induces injury at high shear areas within the artery, e.g., bifurcations, from friction, and induces injury at low shear areas within the artery from oscillatory fatigue. As a result the intima responds to these injuries by thickening and hardening, e.g., callus (commonly called plaque) develops, thereby resulting in arterial clogging or atherosclerosis.
All of the above described stress-induced effects are progressive and irreversible, unless some attempt is made to mechanically and/or pharmacologically correct the pressure/flow/time characteristics of the bolus flow, i.e., the pathology-inducing pulsatile flow must be eliminated or reduced.
It is recognized that the use of certain drugs or pharmaceutical, e.g., calcium channel blockers, beta blockers, etc., can modify the ejection characteristic of the left ventricle. However, such action commonly results in decreased cardiac output and significant clinical side effects.
No mechanical devices have been provided or proposed heretofore for correcting the injury producing pressure/flow/time characteristics of left ventricular ejection. Various devices, however, have been described in the patent literature for assisting cardiac output. For example, numerous types of active, intra-aortic balloon devices have been developed to assist the failing heart in pumping blood. Examples of such devices are disclosed in U.S. Pat. Nos. 3,504,662 (Jones); 3,585,983 (Kantrowitz); 3,692,018 (Goetz et al.); 3,769,960 (Robinson); 4,051,840 (Kantrowitz et al.); 4,685,446 (Choy); 4,741,328 (Gabbay); 4,861,330 (Voss); 4,902,272 (Milder et al.); 4,931,036 (Kanai et al.); and 4,994,018 (Saper).
A need thus exists for a methodology and means for correcting the injurious pressure/flow/time characteristics of the bolus flow.